Pretreatment with ?-Boswellic Acid Improves Blood Stasis Induced Endothelial Dysfunction: Role of eNOS Activation.
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ABSTRACT: Vascular endothelial cells play an important role in modulating anti-thrombus and maintaining the natural function of vascular by secreting many active substances. ?-boswellic acid (?-BA) is an active triterpenoid compound from the extract of boswellia serrate. In this study, it is demonstrated that ?-BA ameliorates plasma coagulation parameters, protects endothelium from blood stasis induced injury and prevents blood stasis induced impairment of endothelium-dependent vasodilatation. Moreover, it is found that ?-BA significantly increases nitric oxide (NO) and cyclic guanosine 3', 5'-monophosphate (cGMP) levels in carotid aortas of blood stasis rats. To stimulate blood stasis-like conditions in vitro, human umbilical vein endothelial cells (HUVECs) were exposed to transient oxygen and glucose deprivation (OGD). Treatment of ?-BA significantly increased intracellular NO level. Western blot and immunofluorescence as well as immunohistochemistry reveal that ?-BA increases phosphorylation of enzyme nitric oxide synthase (eNOS) at Ser1177. In addition, ?-BA mediated endothelium-dependent vasodilatation can be markedly blocked by eNOS inhibitor L-NAME in blood stasis rats. In OGD treated HUEVCs, the protective effect of ?-BA is attenuated by knockdown of eNOS. In conclusion, the above findings provide convincing evidence for the protective effects of ?-BA on blood stasis induced endothelial dysfunction by eNOS signaling pathway.
SUBMITTER: Wang M
PROVIDER: S-EPMC4611516 | biostudies-literature | 2015
REPOSITORIES: biostudies-literature
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